New Study Re Aerolized Cyanobacteria As A Possible Risk for ALS

The health risk of toxic cyanobacteria has primarily been researched in relation to the ingestion of water either by drinking or submersing in contaminated water or eating animals with the toxin found in their organs. Very little research has been done on the possible health risks from aerolized particles from toxic cyanobacteria. There have been a few other studies that have proposed the idea that cyanobacteria might be one of factors in developing ALS, Alzheimer’s and other neurodegenerative diseases, but no definitive findings have been made.

This study provides additional data to show how toxic cyanobacteria may enter the body without requiring the bacteria to make contact with the body through drinking water, eating contaminated food or contact with skin on the outside of the body. These new findings may encourage further research to see if this environmental toxin in an aerolized form could have an impact on the development of ALS or other illnesses.

Identifying Aerosolized Cyanobacteria as an Environmental Risk Factor for ALS using Human Bronchoalveolar Lavage and Nasal Swab Specimens
Objective: To determine if aerosol is a potential route of cyanobacteria (CB) exposure in humans, and a possible risk factor for neurodegeneration in amyotrophic lateral sclerosis (ALS). . . .

Conclusions: These data suggest that humans may inhale aerosolized CB which can be harbored in the nostrils and, in some cases, the lungs. This is consistent with the hypothesis that aerosol may be a significant route of CB transmission. With chronic exposure, we postulate that this could represent an environmental risk factor for ALS.

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Note - title and text edited to correct where the word Alzheimer’s had been used instead of ALS.

@Hip - Thank you for letting me know of my error, I will edit the title and thread.

Yes, it was definitively one of those sad cognitive moments. In my head I was typing ALS, but my fingers (and I guess a short circuit in my brain matter) had me type out Alzheimer’s. I even read the post over and over because it felt like I had spelled something wrong and I just could not see what it was, but I would always end up on the word “Alzheimer’s”. There have been previous studies about the hypothesis that toxic cyanobacteria from bodies of fresh water could be a link to Alzheimer’s. So perhaps in my tangled web of neurons one word beat out others to swim to the surface of my cognitive fog.

In my view of ME/CFS, I find it to contain the same early progression as I've outlined as ALS and Alzheimer's as well. amyloid-B is carried out by LRP-1 protein. The clearance mechanism is not working which leads to abnormal deposition of Aβ in brain cells. This study below links copper in the clearance of Aβ. Copper is normally blocked by the blood-brain-barrier (BBB), but accumulation of copper in blood vessels in the brain can, over time, cause damage to the blood brain barrier, letting copper atoms enter the brain tissue. Copper also disrupts the function of LRP-1 proteins, reducing the removal of Aβ from the brain, which leads to increased protein misfolding and cell damage.

• The most common form of familial ALS (fALS) is linked to a mutation in the SOD1 gene, which codes the SOD1 enzyme (Wikipedia: http://en.wikipedia.org/wiki/SOD1): – SOD1 (superoxide dismutase) is responsible of binding copper and zinc ions. - Another one I need to add to possible links for ME/CFS in my view.

Sparks and Schreurs, in a published 2003 study, found that the addition of only 0.12 parts per million of copper to the drinking water of rabbits greatly enhanced the AD-type pathological changes in the brain, along with marked decrease in performance of previously learned tasks. They also later found that copper in drinking water at even 1/10 the U.S. EPA limit destroyed the blood-brain barrier receptors (LRP receptors) responsible for clearing amyloid beta from the brain, resulting in the hallmark accumulation of amyloid plaques.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC196927/https://www.tandfonline.com/doi/full/10.1080/10937404.2010.499732?src=recsys

In Alzheimer's disease, the hippocampus is one of the first regions of the brain to be affected, leading to the confusion and loss of memory so commonly seen in the early stages of the disease.” ~Dr. Ananya Mandal.
Copper antagonizes zinc, and we know that zinc deprivation causes cell death in the hippocampus, where memories are recorded.

Not sure if this article has been posted elsewhere, but it provides some interesting information on studies that are being conducted on 100 year old toxic algae samples to use as a baseline. From this baseline researchers are hoping that they will be able to see if evolving environmental changes have increased exposure to this toxin and in turn could provide evidence linking the toxin to increased neurodegenerative illnesses (such as ALS and Alzheimer’s). See, https://www.usnews.com/news/healthi...earchers-on-forefront-of-combating-alzheimers

@datadragon - As you can see from my previous posts my brain is rather cognitively challenged. I have been in a significant relapse for the last 2 1/2 months and only recently have I been feeling like some of the gears in my brain are starting up again. So I apologize upfront if my question or comments don’t make sense or they have been asked and answered elsewhere, but I am trying to understand your comments about copper and amyloid-B.

Since ME it is not always a progressive illness, but often a remitting and relapsing illness, do you have a theory on how copper and amyloid-B would cause a different outcome in ME vs. ALS or Alzheimer’s? Do you think MS would also fall into to your copper theory? How would the copper theory explain cluster outbreaks that were appearing in the 1980’s thousands of miles apart?

It does appear from reviewing historical data that significant problems with blue green algae were happening during some of the cluster outbreaks of ME. An environmental toxin can also make other pathogens more difficult or virulent for the immune system to handle, but it still seems that there are more illusive pieces to this puzzle.

A low level of usable copper is common in those with MS and Parkinson's Disease. Myelin is a protective coating on neurons that is progressively lost in patients with MS, due to abnormal immune system attacks that destroy the myelin sheath. As myelin degerates, neuronal function is destabilized and cell death ultimately results, contributing to disease progression and disability in MS patients. Here the NIH wants to study how the deficient levels of copper cause damage to the protective coating.https://multiplesclerosisnewstoday....rosis-study-into-copper-role-in-demyelination

One thought with ME/CFS so far is that in adrenal fatigue/exhaustion we are losing the copper/iron protection that fights common mycotoxins as well as supression of TH1 immunity etc allowing viruses to reactivate, as well as infections to take hold.https://forums.phoenixrising.me/index.php?posts/982375/

The antioxidant, N-acetyl cysteine (NAC), almost completely rescued LRP1 from Copper induced down-regulation it says in the first linked study above regarding alzheimer's. Cucurmin was mentioned in the other study to help with the accumulation of amyloid plaques and reduces amyloid.